• Product name
  • Description
    Rabbit polyclonal to Dynamin 2
  • Host species
  • Tested applications
    Suitable for: ELISA, WBmore details
  • Species reactivity
    Reacts with: Mouse, Human
  • Immunogen

    3 synthetic peptides (human) conjugated to KLH

  • Positive control
    • HeLa cell extracts.



Our Abpromise guarantee covers the use of ab82826 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
  • Application notes
    ELISA: Use at an assay dependent dilution. Antibody specificity was verified by direct ELISA against the 3 immunogen peptides. A minimum titer of 1/90000 is determined for one of the three peptides.
    WB: 1/100. Detects a band of approximately 98 kDa (predicted molecular weight: 98 kDa).

    Not yet tested in other applications.
    Optimal dilutions/concentrations should be determined by the end user.
  • Target

    • Function
      Microtubule-associated force-producing protein involved in producing microtubule bundles and able to bind and hydrolyze GTP. Most probably involved in vesicular trafficking processes, in particular endocytosis.
    • Tissue specificity
      Ubiquitously expressed.
    • Involvement in disease
      Defects in DNM2 are a cause of centronuclear myopathy autosomal dominant (ADCNM) [MIM:160150]; also known as autosomal dominant myotubular myopathy. Centronuclear myopathies (CNMs) are congenital muscle disorders characterized by progressive muscular weakness and wasting involving mainly limb girdle, trunk, and neck muscles. It may also affect distal muscles. Weakness may be present during childhood or adolescence or may not become evident until the third decade of life. Ptosis is a frequent clinical feature. CNMs comprise a wide spectrum of phenotypes, ranging from severe neonatal to mild late-onset familial forms. The most prominent histopathologic features include high frequency of centrally located nuclei in muscle fibers not secondary to regeneration, radial arrangement of sarcoplasmic strands around the central nuclei, and predominance and hypotrophy of type 1 fibers.
      Defects in DNM2 are the cause of Charcot-Marie-Tooth disease dominant intermediate type B (CMTDIB) [MIM:606482]. Charcot-Marie-Tooth disease (CMT) is a clinically and genetically heterogeneous disorder of the peripheral nervous system, characterized by progressive weakness and atrophy, initially of the peroneal muscles and later of the distal muscles of the arms. CMTDIB is a form of Charcot-Marie-Tooth disease characterized by clinical and pathologic features intermediate between demyelinating and axonal peripheral neuropathies, and motor median nerve conduction velocities ranging from 25 to 45 m/sec.
    • Sequence similarities
      Belongs to the dynamin family.
      Contains 1 GED domain.
      Contains 1 PH domain.
    • Cellular localization
      Cytoplasm. Cytoplasm > cytoskeleton. Cell junction > synapse > postsynaptic cell membrane > postsynaptic density. Cell junction > synapse. Microtubule-associated. Also found in the postsynaptic density of neuronal cells.
    • Information by UniProt
    • Database links
    • Alternative names
      • CMT2M antibody
      • CMTDI1 antibody
      • CMTDIB antibody
      • DI CMTB antibody
      • Dnm2 antibody
      • DYN II antibody
      • DYN2 antibody
      • DYN2_HUMAN antibody
      • Dynamin II antibody
      • Dynamin-2 antibody
      • Dynamin2 antibody
      • DynaminII antibody
      • DYNII antibody
      see all


    • Anti-Dynamin 2 antibody (ab82826) at 1/100 dilution + HeLa cell extract

      Anti-Rabbit IgG HRP at 1/1000 dilution

      Predicted band size: 98 kDa
      Observed band size: 98 kDa
      Additional bands at: 75 kDa. We are unsure as to the identity of these extra bands.

    • Anti-Dynamin 2 antibody (ab82826) at 1/100 dilution + HeLa cell extract

      Predicted band size: 98 kDa
      Observed band size: 98 kDa


    ab82826 has not yet been referenced specifically in any publications.

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